Project Summary/Abstract Health is not randomly distributed across people or across space: it tracks a socioeconomic gradient that extends from individuals to the areas in which they live. Individual- and area-level attributes of socioeconomic disadvantage confer risk for a broad range of interrelated physical and neurocognitive health outcomes. This risk is especially apparent in midlife when pathophysiological trajectories of neurocognitive aging that predict risk for dementia in later life begin to accelerate. In this regard, we have provided some of the first evidence that individual- and area- level socioeconomic disadvantage associate with reduced cortical tissue volume and white matter integrity, aspects of brain morphology that show normative shrinkage and integrity loss with age in association with poorer cognitive outcomes. Pathways linking socioeconomic disadvantage to accelerated neurocognitive aging remain unclear. Recent evidence, including our own, suggests that metabolic factors may play a role. Individuals who develop metabolic syndrome, pre-diabetes or type 2 diabetes mellitus are at increased risk for accelerated neurocognitive aging. Furthermore, our recent cross-sectional findings suggest that metabolic risk factors contribute to the associations of area-level disadvantage with brain morphology among midlife adults. Here, we aim to extend this work by longitudinally examining metabolic pathways linking individual- and area-level disadvantage to neurocognitive aging across a 10 year period of midlife. For this purpose, we propose reassessing a sample of 300 cognitively normal midlife adults on whom we collected baseline measures of socioeconomic parameters, metabolic risk, brain morphology and cognitive function 9-10 years ago (mean age at follow-up = 52). Our primary aims examine whether individual- and area-level measures of socioeconomic disadvantage predict changes in brain morphology and cognitive function that decline with age and whether associations of disadvantage with neurocognitive aging are explained by metabolic risk and associated inflammation. We anticipate that this study will contribute to new knowledge to the neurobiology of disparities in cognitive aging.